Biomechanics and muscle function during gait

Gait disorders in patients with cerebral palsy (CP) initially lead to functional deformities which later become structural. The deformities may greatly increase energy consumption and thus limit function. Under normal conditions, however, energy consumption is optimal [1]. Correction of biomechanics towards normality improves energy consumption [2, 3]. For this reason, correction of deformities aims at normality. As, in principle, normal function rather than normal anatomy is the goal, biomechanics and muscle function need to be understood in normal and pathological situations. Gait analysis has yielded deep insights into these issues. Kinematics show the interplay of joint movements at a given time, but only the additional use of kinetics can help us to understand muscle function. A major problem in this respect is the anatomical bias of agonist–antagonist interplay: the main motors of motion. When interpreting kinetic gait data, it becomes obvious that this approach applies poorly to the functional situation. Joint moments are, to a great extent, the product of the ground reaction force (GRF) times its distance to the center of the joint. However, segment inertia and acceleration also contribute and should not be underestimated. The external moment is neutralized by an internal moment created by the muscles on the opposite side of the joint in order to maintain stability. As a consequence, under load, the functional antagonist to the muscle is the external moment. Thus, hip flexion (for instance) may not be due to hip flexor activity. The external moment may flex the hip and inadequate hip extension thus results from hip extensor weakness. In this case, the extensor side of the joint needs to be addressed. Another consequence concerns the direction of muscle activity. Anatomically, a muscle pulls from insertion to origin, moving the distal body segment towards the proximal one. Under load, however, the distal body segment is the more stable of the two segments, as it is relatively fixed to the floor; the proximal one has more freedom of movement. This condition inverts the direction of muscle pull, and the proximal segment moves with respect to the distal one. Thus, the interpretation differs depending on whether a loaded (stance phase) and unloaded (swing phase) situation is considered. One example of such a situation is internal rotation of the leg (seen as hip internal rotation) resulting from excessive dorsiflexion in the subtalar joint and the midfoot. Foot dorsiflexion is a compound movement of the ankle, subtalar, and midfoot joints. The contribution of each joint varies and depends on the length of the triceps surae muscle–tendon complex. The result is an oblique dorsiflexion axis that combines pure dorsiflexion with external rotation and pronation with respect to a fixed shank. If, however, the foot is fixed to the floor by loading and friction, the same movement rotates the leg internally [4, 5]. When the hip flexes and adducts, the pelvis also rotates and tilts anteriorly. This phenomenon becomes more important as the triceps surae shortens and the the midfoot break becomes more pronounced. Severe cases present with a malalignment syndrome. Under normal conditions, however, adequate activity of the tibial muscles stabilizes the foot, avoiding this phenomenon. Another physical effect was described as a plantar flexion–knee extension couple [6, 7]. Only under load is the triceps muscle capable of holding the tibia back and in this way extending the knee (Fig. 1). Due to joint connections and inertia, the effect of this single muscle only travels proximally and leads to hip flexion, internal rotation, and adduction, together with R. Brunner (&) E. Rutz Basel, Switzerland e-mail: reinaldbrunner@sunrise.ch